Although coronary angioplasties have been carried out widely as a treatment for coronary artery diseases, restenosis is a large problem (McBride W, Lange R A, Hillis L D. Restenosis after successful coronary angioplasty. Pathophysiology and prevention. N Engl J Med 1998;318:1734-7). The use of intra-coronary stents reduces the incidence of restenosis, however, restenosis is still observed in 10 to 20% (Serruys P W, de Jaegere P, Kiemeneij F, et al. A comparison of balloon-expandable-stent implantation with balloon angioplasty in patients with coronary artery disease. Benestent Study Group. N Engl J Med 1994;331:489-95.). A number of clinical and angiographic findings, including hypertension, diabetes mellitus, hyperlipidemia, unstable angina, severe coronary artery stenosis and long stenosis lesions, have been reported to be associated with an increased risk of restenosis after coronary angioplasty (Hirshfeld J W Jr, Schwartz J S, Jugo R, et al. Restenosis after coronary angioplasty: a multivariate statistical model to relate lesion and procedure variables to restenosis. The M-HEART Investigators. J Am Coll Cardiol 1991;18:647-56.; Weintraub W S, Kosinski A S, Brown C L 3rd, King S B 3rd. Can restenosis after coronary angioplasty be predicted from clinical variables? J Am Coll Cardiol 1993;21:6-14.; Stein B, Weintraub W S, Gebhart S P, et al. Influence of diabetes mellitus on early and late outcome after percutaneous transluminal coronary angioplasty. Circulation 1995;91:979-89.; Violaris A G, Melkert R, Serruys P W. Long-term luminal renarrowing after successful elective coronary angioplasty of total occlusions. A quantitative angiographic analysis. Circulation 1995;91:2140-50.). The molecular mechanisms underlying restenosis, however, remain to be elucidated. Intra-coronary ultrasound studies in humans suggest that chronic remodeling (vascular constriction) is the major mechanism of restenosis after balloon dilatation (Mintz G S, Popma J J, Pichard A D, et al. Arterial remodeling after coronary angioplasty: a serial intravascular ultrasound study. Circulation 1996;94:35-43.), whereas neointimal hyperplasia is the most important mechanism in in-stent restenosis (Hoffmann R, Mintz G S, Dussaillant G R, et al. Patterns and mechanisms of in-stent restenosis. A serial intravascular ultrasound study. Circulation 1996;94:1247-54). One approach to preventing the development of restenosis after coronary angioplasty is to identify susceptibility genes. Although genetic epidemiological studies have revealed that several genetic polymorphims, including those of angiotensin-converting enzyme (Amant C, Bauters C, Bodart J-C, et al. D allele of the angiotensin I-converting enzyme is a major risk factor for restenosis after coronary stenting. Circulation 1997;96:56-60.; Ribichini F, Steffenino G, Dellavalle A, et al. Plasma activity and insertion/deletion polymorphism of angiotensin I-converting enzyme: a major risk factor and a marker of risk for coronary stent restenosis. Circulation 1998;97:147-154.), angiotensinogen (Volzke H, Hertwig S, Rettig R, Motz W. The angiotensinogen gene 235T variant is associated with an increased risk of restenosis after percutaneous transluminal coronary angioplasty. Clin Sci 2000;99:19-25.), apolipoprotein E (van Bockxmeer F M, Mamotte C D S, Gibbons F R, Taylor R R. Apolipoprotein e4 homozygosity-a determinant of restenosis after coronary angioplasty. Atherosclerosis 1994;110:195-202.), platelet glycoprotein IIIa (Walter D H, Schachinger V, Elsner M, Dimmeler S, Zeiher A M. Platelet glycoprotein IIIa polymorphisms and risk of coronary stent thrombosis. Lancet 1997; 350: 1217-1219.), and stromelysin-1 (Humphries S, Bauters C, Meirhaeghe A, Luong L, Bertrand M, Amouyel P. The 5A6A polymorphism in the promoter of the stromelysin-1 (MMP3) as a risk factor for restenosis. Eur Heart J 2002;23:721-725.), have been reported to be associated with restenosis after balloon dilatation or in-stent restenosis, the genes that contribute to genetic susceptibility to restenosis remain to be identified definitively.